| Literature DB >> 29189146 |
Lisbell D Estrada1, Luciana Oliveira-Cruz1, Daniel Cabrera2,3.
Abstract
Alzheimer's disease is a neurodegenerative condition affecting millions of people worldwide. Alzheimer's symptoms include memory loss and cognitive decline. Pathologically, the hallmarks of Alzheimer´s are the presence of Amyloid beta-plaques, neurofibrillary tangles, and neuronal loss. Unfortunately, no cure is presently available and current treatments are only symptomatic. Transforming growth factor beta type I (TGF-β1) is a trophic factor involved in neuronal development and synaptic plasticity. Impairment of TGF-β1 signaling is associated with exacerbated Aβ deposition and neurofibrillary tangle formation, which increases neurodegeneration. Aging and chronic inflammation reduce the canonical TGF-β1/Smad signaling, facilitating cytotoxic activation of microglia and microgliamediated neurodegeneration This review gathers together evidence for a neuroprotective role of TGF-β in Alzheimer's disease. Restoring TGF-β1 signaling impairment may be a new pharmacological strategy Alzheimer's treatment. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: Alzheimer´s disease; Smad signaling; Transforming growth factor-β1; amyloid-beta; microglia; neuroinflammation; neuroprotection; oligomers.
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Year: 2018 PMID: 29189146 DOI: 10.2174/1389203719666171129094937
Source DB: PubMed Journal: Curr Protein Pept Sci ISSN: 1389-2037 Impact factor: 3.272